Must be nice to know all there is to know about a subject! I'll bet this doctor "knows" that if a ship gets too close to the edge of the Earth, it will fall off, and that the Sun revolves around the Earth, LOL

I first studied the paper and throw several questions, that I have yet to discuss with some of you to try to solve them. I will also consult with some experts on the subject. Anyhow, and after having "dissected" again the study, I have actually realized that my doubts are actually beyond what it's explained in the paper, in an effort to put together these pieces in order to understand how all this could actually lead to an autoimmune process and finally to the symptoms of CFS.

I have written an article quite similar to that of Joel, in Spanish. I am posting it here for what it may be worth:

There's no need to translate this into English, thanks to the fantastic job Joel and others are doing. However, I enjoyed preparing this drawing in English, and I thought I would share it with you. Maybe some of you can help me out with the interrogation marks I have placed in the sketch, and of course, probably some of you will correct it... It can be funny!

Great work putting something together in Spanish! Nice diagram too! I sent you a PM about this, but in case anyone else in interested, I thought I'd post something general about it here too.

As you've probably seen the paper makes reference to 'unpublished data' a couple of times, so I expect there is more information to come. Also the WPI haven't yet published the video of De Meirleir's recent talk, titled "ME/CFS: from Infectious Disease to Autoimmune Disorder". I think they will post it on their blog once the other paper is published. That no doubt will give us some of the details we crave!

However, they have already published a general summary on their blog, in which they mention Th17 cells which are immune cells linked to several other autoimmune conditions, MS, RA, Crohns, etc.

The blog also mentions aberrant protein conformation which I'm not that clued up on yet, but in short: proteins expressed by cells do various tasks and to do those tasks each proteins forms a specific structure. but proteins can sometimes form an incorrect structure and when that happens the protein may have modified functionality. I guess there is room for this to be part of the cause of autoimmunity, but I’m just guessing on that.

If it is autoimmune then it is likely that B cells are affected and I think it is interesting that the Mella and Fluge study using Rituximab reported improvement in about the same proportion of patients as were found to have HERV proteins in this study from De Meirleir and Lombardi.

ME shares many characteristics with known autoimmune diseases, such as a higher occurrence in females than men, improved symptoms during pregnancy, immune dysfunction, family history of autoimmunity etc. Add to that the link with pathogens such as EBV that are thought to play a role in autoimmunity, and now HERVs being found in major antigen-presenting cells...

For me, the increased number of women with ME compared to men is the most striking link. I think it is most likely down to genetics, specifically the X chromosome but it's not out of the question that it is hormonal, or a bit of both.
This new study on MS talks about an increased DNA copy number of HERV-W in MS. Which is strongly linked with the pathopysiology of MS via the MSRV.http://www.ncbi.nlm.nih.gov/pubmed/23308264

Even the most commonly accepted cause of autoimmunity, via molecular mimicry is often complex so I don't imagine De Meirleir, Lombardi et al have the whole picture yet, and even acknowledged autoimmune diseases are not understood that well yet. Still, that needn't stop us thinking about it and discussing the possibilities. I don't know if anyone would be interested in an article looking at autoimmunity in general, or not, but if there is enough interest then maybe I'll put something together...

I've put below a link of an article about a specific HERV and MS, some lines from the article and an image expressing the general hypothesis.
Since MS is kind of put forward as a possible model for ME, this could be relevant.
Anyway, i think it's interesting.

These results together with the many othersaccumulated over the past two decades indicate that thisMSRV subtype of the HERV-W family is likely to play a rolein initiating and fueling a pathogenic ’chain reaction’ causingMS.Based on the present observations and on the preclinicalefficacy of an anti-Env neutralizing monoclonal antibodyin MS-like EAE animal models induced by HERV-W Env,as evoked above in this discussion, a humanized antibody isnow to be evaluated in clinical trials with MS patients(Clinical Phase I has been achieved).

It has been proposed that SAgs might contribute to the pathogenesis of autoimmune disease by activating T cells that are specific for self antigens. Although there is no direct evidence of SAg involvement, it has been suggested that SAgs could, under the right conditions, break the tolerance or suppression of auto-reactive T cell clones and induce a state of autoimmunity. Evidence for this hypothesis came from an animal model of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE), where it was shown that administration of SEB to mice recovering from EAE triggered direct stimulation of the Vβ3 positive auto-reactive MBP peptide specific T cells resulting in a rapid relapse of the disease [73,74].
Conrad and colleagues found a biased TcR usage in T cells from IDMM patients towards Vβ7 suggesting the activity of a SAg [58]. They showed that the mitogenic activity was encoded by a gene residing on an endogenous retrovirus, named IDDMK1,222 and that viral expression occurred only in IDMM patients. It was shown later by the same group that IDDMK1,222 is identical to one allele of the EBV-inducible HERV-K18 carrying the Vβ7-specific SAg K18·3 [56] (see above)." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808794/[my bolding]

I would like to point out though that if we have LPS in the blood, and we have any of the bacteria or viruses that produce superantigens, then superantigens will likely get into our general circulation as well - LPS is a marker of detox failure in my opinion. Staph aureus is the classic superantigen producer, but it is far from alone. Various staph and strep bacteria produce these. Its also worth noting that we tend to have chronic staph or strep nasal infections. Even mycobacteria make them. EBV is thought to have a superantigen.

I am interested in gamma delta T cells due to their super sensitivity to bacterial toxins/markers and their function in suppressing excess immune stimulation. They activate or deactivate the immune system, talk to dendritic cells, and accelerate wound healing.

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Very interesting post Alex, my IL17 is sky high ( as is my CD14s), so the gamma delta T cells and autoimmunity connection looks like a potent area for research for those pwME whose disease is gut based.

Can I add - on the gender bias it does not seem to be so in my case. I (UK) went down first and brother (US) went down a year later. His even more severe than my own severities apparently exhibiting more dangerous latent viruses such as JCV (think that's the one - affects the brain).

Can I add - on the gender bias it does not seem to be so in my case. I (UK) went down first and brother (US) went down a year later. His even more severe than my own severities apparently exhibiting more dangerous latent viruses such as JCV (think that's the one - affects the brain).

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Interesting, JCV infects the GI tract as well as the brain. I think i read/heard somewhere about autoimmune conditions presenting more severely in the men that do get them too.

According to their newsletter yesterday, they are still looking. I think it may have said somethign about findings to be published this year, but i may have imagined that bit as it was late and I was only skimming it.

She said that she had studied plasma dendritic cells of MECFS patients and to her surprise "none of them" were pumping out interferon (as they should do). Obviously that represents severe immune dysfunction and it suggested a retroviral infection of the cells, because it is known that HTLV1 prevents plasma dendritic cells from producing interferon.
Shame that research may never see the light of day.

She said that she had studied plasma dendritic cells of MECFS patients and to her surprise "none of them" were pumping out interferon (as they should do). Obviously that represents severe immune dysfunction and it suggested a retroviral infection of the cells, as this paper is hinting at, because it is known that HTLV1 prevents plasma dendritic cells from producing interferon.
Shame that research may never see the light of day.

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Actually WPi has issued a paper last year or 2013 about plasmacytoid demdritic cells. i forgot what was the conclusions.